Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

The renal growth hormone--insulin-like growth factor-I system in acute ischemic renal failure. Recovery from acute tubular necrosis (ATN) is accelerated by IGF-I therapy. Furthermore, the local renal growth hormone-IGF-I system may participate in the natural repair. We examined the IGF-I system in rat kidneys subjected to 60 minute ischemia compared to sham operated controls. Two days after injury, growth hormone receptor mRNA and IGF-I mRNA levels fell approximately 9 to 33% of control values. This was associated with a reduction in kidney immunoreactive IGF-I levels. In contrast, IGF-I receptor mRNA abundance was unchanged. However, plasma membrane IGF-I receptor binding on day 2 and day 7 was near double the control values (P < 0.01). Scatchard analysis revealed a near twofold increase in receptor number. Since receptor mRNA levels were unchanged, this implies receptor protein up-regulation. In contrast to unchanged IGF-I receptor mRNA levels, the abundance of mRNA levels of insulin-like growth factor binding proteins (IGFBP) -2, -3, -4 and -5 fell approximately 14 to 62% of control levels day 2 after injury (P < 0.05), suggesting reduced IGFBP production. Thus, the renal response to ischemic ATN, namely, low IGFBP mRNA levels and high IGF-I receptor number, may function to increase IGF-I bioavailability and thereby enhance the reparative actions of local and circulating IGF-I in ischemic ATN.
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PMID:Renal growth hormone--insulin-like growth factor-I system in acute renal failure. 754 60

As acute tubular necrosis (ATN) is still an important cause for postoperative malfunction of renal grafts, it would be useful to have a method predicting such a complication. We investigated the possibility to predict ATN by measuring the ratio of phosphomonoesters (PME, largely consisting of adenosine monophosphate) and inorganic phosphate (Pi) in the renal tissue, using 31P magnetic resonance spectroscopy (MRS) during the cold ischemia period. Assuming that this ratio reflects the tissue high-energy phosphate status, we studied five kidneys from living related donors (LRD), 28 kidneys from heart beating donors (HBD) and nine kidneys from non-heart beating donors (non-HBD). All kidneys were preserved with a phosphate free solution. We found an inverse relation between the time of 31P MRS and the PME/Pi ratio, suggesting a graded decay of tissue high energy phosphates during cold ischemia. The PME/Pi ratio was highest in grafts from LRD (2.65 +/- 0.50, no ATN), intermediate in grafts from HBD (1.65 +/- 0.41, 21% ATN) and lowest in those derived from non-HBD (1.05 +/- 0.47, 56% ATN). The differences in PME/Pi ratio between the groups was statistically significant (P < 0.01). Moreover, the ratio was significantly lower in grafts developing ATN (1.73 +/- 0.41 vs. 1.35 +/- 0.29 in the HBD group, 1.41 +/- 0.24 vs. 0.76 +/- 0.36 in the non-HBD group, P < 0.05). These observations point to a general relation between the pre-transplant kidney PME/Pi ratio and the development of ATN. However, the predictive value of a low PME/Pi ratio was too low (36%) to reliably predict development of ATN in individual cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pre-transplantation assessment of renal viability with 31P magnetic resonance spectroscopy. 770 29

Contrast-enhanced perfusion patterns of newly transplanted kidneys were determined in 10 patients. Albumin-stabilized sonicated microspheres were injected into the iliac-renal artery of the transplanted kidney while continuous two-dimensional ultrasound images were recorded. Doppler derived resistance index (RI) of the transplanted kidney's blood flow before injection of contrast (0.68 +/- 0.8) did not differ significantly from RI measured immediately after injection (0.72 +/- 0.13) or RI 24 h after surgery (0.69 +/- 0.11). Heart rate, mean arterial pressure, central venous pressure, and electrocardiogram (ECG) signs for ischemia did not change during contrast injections. Renal scintigraphy and renal biopsy revealed acute tubular necrosis and/or rejection in two patients at 24-48 h. Videodensitometry was used to assess the ratio of inner to outer peak pixel intensity from the recorded tomographic images in six patients. In both patients with acute rejection, the inner to outer cortex peak pixel intensity was greater than 1, whereas it was less than 1 in the remaining four patients with normal postoperative renal function. Visual scores (0-3) of contrast enhancement for three doses of Albunex were evaluated (0.5 mL, 1.0 mL, 2.0 mL). Two milliliters always enabled perfusion assessment. In seven patients the identical dose of Albunex was injected immediately before and 30 s after 2 mg of verapamil was injected directly into the renal artery at the time of surgery. The contrast enhancement score before verapamil (1.4 +/- 0.6) was significantly less than the enhancement score after (2.1 +/- 0.6), implying greater renal blood flow after verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and feasibility of renal blood flow determination during kidney transplant surgery with perfusion ultrasonography. 781 23

Poor initial function is common in cadaveric renal transplantation, and is usually attributed to acute tubular necrosis (ATN) brought about by ischemia during harvesting/implantation. However, this is often an assumption rather than a specific diagnosis. Recently, in 4 kidneys from 2 cadaver donors, we found evidence of severe endothelial injury, prior to exposure to cyclosporine or other known endothelial toxins. The biopsies at the time of completion of the transplant revealed apparent loss of glomerular endothelial cells on light microscopy, corresponding on electron microscopy to shrinkage of the endothelial cells away from the basement membranes of the capillary loops. Extensive microvascular thrombi were present. All 4 grafts displayed impaired initial function, which partially recovered with time. The finding of these unusual lesions in both kidneys from each of 2 donors suggested donor factors, although the only factor common to both donors was massive brain disruption. Thus, in the differential diagnosis of poor initial function in kidneys transplanted from cadaver donors, one should consider renal endothelial injury, which could lead to microthrombus formation, abnormal vasomotion, and functional impairment in the transplant.
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PMID:Glomerular endothelial cell detachment in paired cadaver kidney transplants: evidence that some cadaver donors have pre-existing endothelial injury. 801 21

To elucidate the role of apoptosis and cell desquamation in the repair phase of acute tubular necrosis, morphological findings after 60 min ischaemia were investigated in rats. A morphometric analysis of the cell proliferation and of the epithelial cellularity of reconstructing tubules was performed. The kinetics of apoptosis and cell desquamation were also examined. Ischaemia and reperfusion injury resulted in widespread necrosis of tubules at day 1. Subsequently, a regenerative epithelial hyperplasia took place in the early stage. The most marked increase in cellularity in the damaged tubules was on day 6, when the tubules became lined by hyperplastic epithelial cells with papillary clusters. The number of papillary clusters decrease up to day 8, and during this period many desquamated cells from the clusters were observed in the tubular lumen. In the later stage, hyperplastic epithelial cells were reduced to their original cellularity and during this period the number of apoptotic cells obviously increased, while the damaged tubules were reconstructed. We conclude that epithelial overproduction occurs in the early phase after tubular necrosis, and excess hyperplastic epithelial cells regress during the repair process by cell desquamation and apoptosis, both of which are essential for the recovery of the original tubular structure.
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PMID:Apoptosis and cell desquamation in repair process of ischemic tubular necrosis. 824 76

This study evaluated renal function and histological and oxidative injury in transplanted kidneys harvested after prolonged warm ischemia in pigs. In 8 donor pigs, kidneys were perfused in situ 120 min after cardiac arrest. One of each pair of kidneys was used for histological and biochemical studies while the other was transplanted into a recipient undergoing bilateral nephrectomy. In 6 cases, renal function was satisfactory 14 days after transplantation. Histologically, a reversible acute tubular necrosis was observed with partial recovery at the 14th postoperative day. A moderate oxidation was revealed by decreased glutathione and increased malondialdehyde levels. In spite of this ischemic injury, these findings suggest that kidneys harvested after prolonged warm ischemia can still recover after transplantation, and that non-heart-beating donors may be considered as an alternative organ source for kidney transplantation.
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PMID:Transplantation of warm ischemia damaged kidneys: an experimental study in pigs. 829 Jul 3

We reviewed a series of 500 transplants and found 21 (4.1%) cases of graft rupture. All the renal grafts had been harvested from cadavers. Hemodialysis was required in 18 (85%), acute rejection developed in 12 and acute tubular necrosis in 12 (3 were related to percutaneous maneuvers for biopsy or PCN). All cases developed acute pain and oligoanuria. No significant difference was observed relative to ischemia time or HLA typing. Concerning immunosuppression and graft rupture, a significant difference was observed for the group that received low dose CsA combined with triple therapy (3 rupture grafts, 14.2%) versus the high dose CsA and steroid treated group (11 ruptured grafts, 52.3%), p < 0.01. Twenty grafts had ruptured within the first 15 days following transplantation and one at 8 months. Graft removal was warranted in 8 (38%) and conservative surgery in 12 (57%). Two grafts (16%) were lost and 1 patient (4.7%) died without undergoing surgery. Graft rupture is a severe complication that warrants immediate surgical management. Conservative surgery is a valid alternative in those cases with a viable graft.
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PMID:[Spontaneous rupture of transplanted kidney. Experience with 500 transplants]. 833 69

Imaging of the renal, hepatic, and pancreas allograft is essential for evaluation of postoperative complications. Surgical complications after organ transplantation can generally be specifically diagnosed. These complications include obstruction, leakage, peritransplant fluid collections, and vascular problems such as vascular stenosis or thrombosis, arteriovenous fistula, and pseudoaneurysm. Using computed tomography (CT) or ultrasound guidance, interventional procedures can often be performed to treat various surgical complications. On the other hand, medical causes of allograft transplant dysfunction such as rejection, acute tubular necrosis, drug toxicity, ischemia, infection, inflammation, or the development of recurrent disease are frequently associated with nonspecific imaging findings. Allograft biopsy is still usually necessary for definitive diagnosis in these cases. In this article, we will briefly outline the spectrum of abnormalities that can be seen in the allograft recipient and show some examples of these complications.
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PMID:Imaging of the kidney, liver, and pancreas transplant. 835 33

For many years Doppler ultrasound has helped to identify the cause of renal allograft dysfunction. However, Doppler examinations were often performed after the onset of acute renal failure. In the present study we used Doppler ultrasound during grafting to follow changes in renovascular resistance. As early as 30 min after the renal artery had been unclamped, the calculated resistance index (RI) at the hilar part of the renal artery was significantly higher in the group of patients who developed acute tubular necrosis (ATN) than in the group of patients with early normalization of renal function (P = 0.05). This result did not correlate with raised cold and warm ischemia times and serum creatinine level on discharge in patients who presented with ATN. RI higher than 0.730 min after unclamping allows for an identification of those grafts at greater risk for the development of ATN and should be an indication for the early introduction of intensive therapy.
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PMID:The use of perioperative Doppler ultrasound as a screening test for acute tubular necrosis. 845 26


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